For example, tau filaments from the AD brain (consisting of both 3R and 4R isoforms) contained only R3, R4, and a part of the C‐terminal region, distinct from those from Pick's disease (PiD; 3R tauopathy) and CBD (4R tauopathy).[5] Furthermore, the recombinant tau fragments, consisting of 2N4R tau residues 306–378 (hereafter named tau‐AC), spontaneously assembled and further induced endogenous tau aggregation.[6] However, the underlying mechanisms driving this phenomenon and its pathophysiological implications in AD remain largely uncharacterized. This evidence concerns the gene MAPT and pelvic inflammatory disease.